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19. Editorial Acknowledgment

Author

Aarvak, T., Abedi-Valugerdi, M., Abrahamsen, T., Akdis, C., Akuffo, H.O., Alarcon-Riquelme, M., Andersen, P., Arstila, P., Austgulen, R., Baecker-Allan, C., Baggiolini, M., Baker, B.S., Bakke, O., Bakken, V., Barclay, A.N., Bemark, M., Benestad, H.B., Berzins, K., Bjerkvik, R., Bjørge, L., Bland, P., Bolstad, A.I., Born, W., Bowman, S., Brinchmann, J., Britton, S., Brokstad, K.A., Brunet, L.R., Bruserud, Ø., Cardona, P.J., Ceyppens, J.L., Cirino, G., Cohn, M., Cox, R.J., Cunliffe, J., Dahlgren, U., Dellacasagrande, J., Ditzel, H., Dobryszycka, E., Dyrhol-Riise, A.M., Edwards, J.C., Egeland, T., Elsayed, S., Eray, M., Erb, K.J., Esch, T., Eugen-Olsen, J., Everse, L.A., Fagerhol, M., Farstad, I., Feldmann, M., Fernandez, C., Fleck, M., Franksson, R., Freitas, A., Garred, P., Gidlund, M., Gilhus, N.E., Goldbach-Mansky, R., Gordon, J., Gordon, T., Grandien, A., Gregerson, P., Grewal, H., Hakulinen, J., Halstensen, T., Haneberg, B., Hanej, S.H.E., Hansen, T., Harley, J.B., Haukenes, G., Hengartner, H., Henz, B.M., Holen, E., Hurme, M., Husby, G., Husby, S., Hörnqvist-Hultgren, E., Haaheim, L.R., Isenberg, D., Jahnson, F., Jakobsen, H., James, J.A., Jansson, J.O., Jarva, H., Jeansson, S., Johannessen, A.C., Johansen, F.E., Julkunen, I., Kalland, K.H., Kaye, J., Kazatchkine, M., Kihlström, E., Kohler, L., Konttinen, Y., Kotenko, S., Koutzov, S., Krammer, P., Kristoffersen, E., Kunzendorf, U., Lachmann, P., Langman, R., Langner, J., Lanzavecchia, L., Lappalainen, M., Laskay, T., Lea, T., Lefvert, A.K., Lehmann, A.C., Louka, A, Lúdviksson, B.R., Mariette, X., Marion, T., Marker-Herrmann, E., Mattsson, R., McAdam, S., Mellbye, O.J., Mellgren, G., Mellgren, S.I., Mestecky, J., Michaelsen, T., Michalek, S., Miettinen, A., Moestrup, S.K., Moretta, A., Moser, M., Mountz, J., Moutsopoulos, H., Munthe, L.A., Mustafa, T., Myrmel, H., Nannemark, G., Netea, M.G., Nilsen, R., Notarangelo, L.D., Ögmundsdóttir, H., Olsson, I., Olweus, J., Osland, A., Paludan, S.R., Parsons, K.R., Patarroyo, M., Paul, W.E., Perlman, P., Pollock, J.M., Puolakkainen, M., Quale, A., Rajewsky, K., Raman, C., Reichlin, M., Renkonen, R., Rese Shadidi, K., Ricciardi-Castagnoli, P., Rickinson, A.B., Ringdén, O., Risto, R., Rodinov, D., Rosenkrands, I., Rottenberg, M., Russel, M., Rygaard, J., Rødahl, E., Röllinghof, M., Sandberg, M., Schenk, K., Seppälä, I., Shevach, E., Shortman, K., Siegrist, C.A., Sigurdardóttir, S., Silvennoinen, O., Sinigaglia, F., Sistonen, L., Skarstein, K., Skogh, T., Smith, E., Spurkland, A., Stendahl, O., Sugden, B., Suri-Payer, E., Svennerholm, A.M., Szodoray, P., Theofilopoulos, A., Thorley-Lawson, D.A., Timonen, T., Trowsdale, J., Tuomo, T., Ulmer, A.J., Ulvestad, E., Ulvik, R., Vaerman, J.P., van, der Merwe J.P., van Eden, W., Vedeler, C., Vintermyr, O.K., Vyse, J., Wahlgren, M., Wahren-Herlenius, M., Walsh, L.J., Weetman, A.P., Westermark, P., Wiker, H., Yang, J., Yewdell, J.W., Youinou, P., and Zouali, M.

Published
2002

33. Malignancy: Insulin-like Growth Factor-1 (IGF-1) is a Costimulator of the Expansion of Lineage Committed Cells Derived from Peripheral Blood Mobilized CD34+ Cells in Multiple Myeloma Patients

Author

STEIN, Frostad, ROBERT, Bjerknes, TOR, Hervig, INGERID, Nesthus, JOHANNA, Olweus, and ØYSTEIN, Bruserud Ø

Abstract

The effect of insulin-like growth factor-1 (IGF-1) on highly enriched human apheresis CD34(+) progenitor cells was investigated in vitro. The progenitor cells were mobilized by treatment with cyclophosphamide + granulocyte - colony stimulating factor (G-CSF) in patients with multiple myeloma. CD34(+) cells were cultured for 7 days in serumfree medium containing stem cell factor (SCF), granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-3 (IL-3), and this is referred to as cytokine-dependent proliferation. After 7 days of cytokine-dependent proliferation the total number of viable cells increased 1.6-8.2 times, and subsets of cells expressing the granulocyte marker CD15, the myelomonocytic marker CD64 and the erythrocyte phenotype CD71(high) /CD64(-) were detected among the in vitro cultured cells. Addition of G-CSF together with SCF + IL-3 + GM-CSF increased the number of CD15(+) and CD64(+) cells, but without altering the number of erythroid cells. IGF-1 caused a dose-dependent increase in the number of CD15(+), CD64(+) and CD71(high) /CD64(-) cells, and this increase was detected when cells were cultured in both SCF + IL-3 + GM-CSF alone and G-CSF + SCF + IL-3 + GM-CSF. A minor subset of CD34(+) cells could still be detected among in vitro cultured cells and the number of CD34(+) cells was not altered by adding G-CSF and/or IGF-1. Morphologically recognizable mature granulocytes or erythroid cells could not be detected for any of the combinations investigated. We conclude that IGF-1 can enhance the in vitro proliferation of committed progenitor cells derived from apheresis CD34(+) cells.

Published
2001

36. Cyclic AMP can promote APL progression and protect myeloid leukemia cells against anthracycline-induced apoptosis

Author

Gausdal, G, primary, Wergeland, A, additional, Skavland, J, additional, Nguyen, E, additional, Pendino, F, additional, Rouhee, N, additional, McCormack, E, additional, Herfindal, L, additional, Kleppe, R, additional, Havemann, U, additional, Schwede, F, additional, Bruserud, Ø, additional, Gjertsen, B T, additional, Lanotte, M, additional, Ségal-Bendirdjian, E, additional, and Døskeland, S O, additional

Published
2013
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